首页> 外文期刊>Neuropeptides: An International Journal >Normalization of circulating leptin levels by fasting improves the reproductive function in obese OLETF female rats.
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Normalization of circulating leptin levels by fasting improves the reproductive function in obese OLETF female rats.

机译:通过禁食使循环瘦素水平正常化可改善肥胖OLETF雌性大鼠的生殖功能。

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In order to examine a possible detrimental effect of hyperleptinemia on the reproductive system, we examined whether a decrease in circulating leptin levels by fasting affects the estradiol/progesterone-induced luteinizing hormone (LH) and prolactin (PRL) surges in genetically obese OLETF (Otsuka-Long-Evans-Tokushima-Fatty) rats. Experiments were performed on both normally fed and 3-day starved groups from ovariectomized OLETF rats and their controls LETO (Long-Evans-Tokushima-Otsuka). Starved LETO rats, whose leptin levels were less than 0.5 ng/ml, did not show a significant surge of either LH or PRL. Normally fed OLETF rats, whose leptin levels were 9.7 +/- 1.8 ng/ml, showed a significant but small surge for both LH and PRL. Interestingly, starved OLETF rats, whose leptin levels (4.1 +/- 0.7 ng/ml) were similar to those in normally fed LETO rats (3.3 +/- 0.4 ng/ml), had significantly greater surges of both hormones than normally fed OLETF group. This study demonstrates for the first time that the normalization of circulating leptin levels in female OLETF rats augments the steroid-induced LH and PRL surges, and also suggests a deleterious effect of hyperleptinemia on the reproductive axis. Copyright 2001 Harcourt Publishers Ltd.
机译:为了检查高瘦素血症对生殖系统的可能有害作用,我们检查了空腹循环中瘦素水平的降低是否影响遗传性肥胖OLETF(Otsuka)中的雌二醇/孕激素诱导的黄体生成激素(LH)和催乳素(PRL)激增-长埃文斯-德岛(Fatty)大鼠。对来自卵巢切除的OLETF大鼠及其对照组LETO(Long-Evans-Tokushima-Otsuka)的正常进食组和3天饥饿组进行了实验。瘦素水平低于0.5 ng / ml的饥饿的LETO大鼠没有表现出LH或PRL的明显升高。瘦素水平为9.7 +/- 1.8 ng / ml的正常喂养的OLETF大鼠对LH和PRL均表现出明显但很小的激增。有趣的是,饥饿的OLETF大鼠的瘦素水平(4.1 +/- 0.7 ng / ml)与正常喂食的LETO大鼠(3.3 +/- 0.4 ng / ml)相似,两种激素的激增均明显高于正常喂食的OLETF。组。这项研究首次证明雌性OLETF大鼠中循环瘦素水平的正常化增强了类固醇诱导的LH和PRL激增,并且还暗示了高瘦素血症对生殖轴的有害作用。版权所有2001 Harcourt Publishers Ltd.。

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